Diabetic retinopathy (DR) is a microvascular complication of diabetes and one of the most common causes of blindness in active stage. This study is performed to explore the effects of microRNA-21 (miR-21) on retinal vascular endothelial cell (RVEC) viability and angiogenesis in rats with DR via the phosphatidylinositiol 3-kinase/protein kinase B (PI3K/Akt)/vascular endothelial growth factor (VEGF) signaling pathway by binding to phosphatase and tensin homolog (PTEN). Sprague Dawley (SD) rats were used for establishment of DR models. Target relationship between miR-21 and PTEN was assessed by bioinformatics prediction in combination with dual-luciferase reporter gene assay. Identification of expression of miR-21, PTEN and PI3K/Akt/VEGF signaling pathway-related genes in the retinal tissues was then conducted. In order to assess the contributory role of miR-21 in DR, the RVECs were transfected with mimic or inhibitor of miR-21, or siRNA-PTEN, followed by the detection of expression of PTEN and PI3K/Akt/VEGF-related genes, as well as the measurement of cell viability, cell cycle and apoptosis. Increased expression of miR-21 and PI3K/Akt/VEGF related genes, along with a reduced expression of PTEN was observed in the retinal tissues of DR rats. PTEN was targeted and negatively regulated by miR-21, while the PI3K/Akt/VEGF signaling pathway was activated by miR-21. RVECs transfected with miR-21 inhibitor exhibited promoted viability and angiogenesis, and inhibited apoptosis. To conclude, our results indicated that miR-21 overexpression could potentially stimulate RVEC viability and angiogenesis in rats with DR through activation of the PI3K/Akt/VEGF signaling pathway via repressing PTEN expression, highlighting the potential of miR-21 as a target for DR treatment.

中文翻译：

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在糖尿病性视网膜病变中，microRNA-21的抑制通过PTEN依赖的PI3K / Akt / VEGF信号通路抑制视网膜血管内皮细胞的生长和血管生成。

糖尿病性视网膜病（DR）是糖尿病的微血管并发症，是活跃期失明的最常见原因之一。进行这项研究以探讨microRNA-21（miR-21）通过磷脂酰肌醇3激酶/蛋白激酶B（PI3K / Akt）/血管内皮细胞对DR大鼠视网膜血管内皮细胞（RVEC）活力和血管生成的影响生长因子（VEGF）信号传导途径，通过与磷酸酶和张力蛋白同源物（PTEN）结合而实现。使用Sprague Dawley（SD）大鼠建立DR模型。通过生物信息学预测结合双荧光素酶报告基因检测评估了miR-21和PTEN之间的靶标关系。然后鉴定视网膜组织中miR-21，PTEN和PI3K / Akt / VEGF信号通路相关基因的表达。为了评估miR-21在DR中的作用，将RVEC用miR-21的模拟物或抑制剂或siRNA-PTEN转染，然后检测PTEN和PI3K / Akt / VEGF相关基因的表达，以及细胞活力，细胞周期和细胞凋亡的测量。在DR大鼠的视网膜组织中观察到miR-21和PI3K / Akt / VEGF相关基因的表达增加，而PTEN的表达减少。PTEN被miR-21靶向并负调控，而PI3K / Akt / VEGF信号通路被miR-21激活。转染了miR-21抑制剂的RVEC表现出增强的生存力和血管生成，并抑制细胞凋亡。总而言之，